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IL-9:FSGS 中一种新的促足细胞存活细胞因子。

IL-9: a novel pro-podocyte survival cytokine in FSGS.

机构信息

Division of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, USA; Department of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.

Division of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, USA.

出版信息

Kidney Int. 2020 Sep;98(3):541-543. doi: 10.1016/j.kint.2020.05.045.

DOI:10.1016/j.kint.2020.05.045
PMID:32828233
Abstract

Progressive focal segmental glomerulosclerosis, characterized by podocyte loss, is often refractory to treatment and leads to progressive proteinuric chronic kidney disease. Interleukin-9 (IL-9) is reported to play important roles in innate and adaptive immunity in extrarenal inflammatory diseases. By using an IL-9 knockout mouse model, Xiong et al. demonstrate IL-9 as a novel pro-podocyte survival cytokine in the adriamycin nephropathy model of focal segmental glomerulosclerosis. Sequential in vitro and in vivo data corroborate a direct protective role, rather than an immunologic role, for IL-9 on podocyte survival. This commentary highlights these novel data and discusses the necessary steps for developing IL-9 as a potential novel therapeutic for focal segmental glomerulosclerosis.

摘要

进行性局灶节段性肾小球硬化症,其特征是足细胞丧失,常对治疗有抗性,并导致进行性蛋白尿性慢性肾脏病。据报道,白细胞介素-9(IL-9)在肾脏外炎症性疾病的先天和适应性免疫中发挥重要作用。熊等人通过使用 IL-9 敲除小鼠模型,证明了 IL-9 是局灶节段性肾小球硬化症阿霉素肾病模型中新型促足细胞存活细胞因子。体外和体内的序贯数据证实了 IL-9 对足细胞存活的直接保护作用,而不是免疫作用。本评论强调了这些新数据,并讨论了将 IL-9 开发为局灶节段性肾小球硬化症潜在新型治疗方法的必要步骤。

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IL-9: a novel pro-podocyte survival cytokine in FSGS.IL-9:FSGS 中一种新的促足细胞存活细胞因子。
Kidney Int. 2020 Sep;98(3):541-543. doi: 10.1016/j.kint.2020.05.045.
2
Interleukin-9 protects from early podocyte injury and progressive glomerulosclerosis in Adriamycin-induced nephropathy.白细胞介素-9可保护阿霉素诱导的肾病中的早期足细胞损伤和进行性肾小球硬化。
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Angiopoietin-like-3 knockout protects against glomerulosclerosis in murine adriamycin-induced nephropathy by attenuating podocyte loss.血管生成素样蛋白3基因敲除通过减轻足细胞丢失来预防小鼠阿霉素诱导的肾病中的肾小球硬化。
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Angiotensin II type-2-receptor stimulation ameliorates focal and segmental glomerulosclerosis in mice.血管紧张素 II 型受体刺激可改善小鼠的局灶节段性肾小球硬化。
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Transcription factor MafB in podocytes protects against the development of focal segmental glomerulosclerosis.足细胞中的转录因子 MafB 可防止局灶节段性肾小球硬化的发生。
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MAD2B-mediated cell cycle reentry of podocytes is involved in the pathogenesis of FSGS.MAD2B 介导的足细胞细胞周期再进入参与 FSGS 的发病机制。
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C-C chemokine receptor type 2 mediates glomerular injury and interstitial fibrosis in focal segmental glomerulosclerosis.C-C 趋化因子受体 2 介导局灶节段性肾小球硬化中的肾小球损伤和间质纤维化。
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CXCL12 blockade preferentially regenerates lost podocytes in cortical nephrons by targeting an intrinsic podocyte-progenitor feedback mechanism.CXCL12 阻断通过靶向固有足细胞祖细胞反馈机制优先在皮质肾单位中再生丢失的足细胞。
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RAGE mediates podocyte injury in adriamycin-induced glomerulosclerosis.晚期糖基化终末产物受体介导阿霉素诱导的肾小球硬化中的足细胞损伤。
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Swollen Feet: Considering the Paradoxical Roles of Interleukins in Nephrotic Syndrome.足部肿胀:探讨白细胞介素在肾病综合征中的矛盾作用
Biomedicines. 2024 Mar 26;12(4):738. doi: 10.3390/biomedicines12040738.
2
New indication of Chuankezhi injection for steroid-resistant focal segmental glomerulosclerosis and its mechanism of action.喘可治注射液治疗激素抵抗型局灶节段性肾小球硬化的新适应症及其作用机制
Ann Transl Med. 2022 Jun;10(11):639. doi: 10.21037/atm-22-1962.
3
Immune-mediated entities of (primary) focal segmental glomerulosclerosis.
(原发性)局灶节段性肾小球硬化的免疫介导实体。
Cell Tissue Res. 2021 Aug;385(2):423-434. doi: 10.1007/s00441-021-03454-3. Epub 2021 Apr 27.
4
Plasma Cytokine Profiling to Predict Steroid Resistance in Pediatric Nephrotic Syndrome.血浆细胞因子谱分析预测儿童肾病综合征的类固醇抵抗
Kidney Int Rep. 2021 Jan 6;6(3):785-795. doi: 10.1016/j.ekir.2020.12.027. eCollection 2021 Mar.